Sabato 27 ottobre 2012 - Pacini Editore

306
liver and adrenal viral localization (presumably Herpes Virus or
CMV) associated with placental mesenchymal dysplasia.
The diagnosis of placental mesenchymal dysplasia is in most
cases clinical; it can sometimes become difficult, only on ultrasound
features, to distinguish it from a partial hydatidiform mole.
Indeed both diseases show cystic parenchyma areas but there is
no increase of serum beta-HCG that occurs only in trophoblast
diseases. This has an histological evidence because PMD is not
due to trophoblast hyperplasia, which is on the other hand present
in partial mole.
Currently, the pathogenesis of PMD is unknown, the evidence
of thrombosis in fetal vessels has led the authors to suggest the
possibility of a maternal thrombophilia. Association with IUGR
and evidence of chorangiosis has instead brought to theorize a
possible role of chronic hypoxia.
However some cases were associated with placental mesenchymal
genetic mosaicism, which would lead to an abnormal development
of the mesenchyme while the surrounding trophoblast is
normal. This is also supported by the association with hamartomas
in some fetuses. These features, added to the association with
Beckwith-Wiedemann syndrome and the female preponderance,
suggest that there may be a mechanism of imprinting.
In our case, obstetricians have excluded maternal thrombophilic
disorders and presence of IUGR; it is thus supposed that there
may have been a sporadic event that led to the development of
this particular disease, which likely would lead to a weakening of
the entire placental apparatus (membranes included) and then to
the occurrence of a untimely rupture of the membranes which is
a well known cause of perinatal fetal infections.
references
1 Beargen R. Miscellaneous placental lesions. In: Manual of pathology
of the human placenta. 2 nd Ed. Springer 2011.
2 Zeng X, Chen MF, Bureau Y-A, et al. Placental mesenchymal dysplasia
and an estimantion of population incidence. Acta Obstet Gynecol
Scand 2012;91:754-7.
3 Avgil M, Ornoy A. Herpes simplex virus and Epstein-Barr Virus
infections in pregnancy: consequences of neonatal or intrauterine
infection. Reprod Toxicol 2006;21:436-45.
Espression of P16 InK4A / KI67 dual-stain cytology
and cytological diagnosis in a population hpv dna-
Hr positive. correlations and histological follow up
L. Borghi, P. Rossi, R. Ferro, M. Zanella, R. Mencarelli
Anatomia Patologica Dipartimento Patologia Clinica, Azienda
Ulss 18, Rovigo
Objective of the study. Cytological diagnosis and co-expression
of p16 INK4a (p16) protein and biomarker Ki67 have been made
on a selected HR-HPV DNA positive population using Hybrid
Capture II method. Correlations among cytological - histological
diagnosis and p16/Ki67 expression patterns, identifying different
classes of risk that need individual follow-up.
Materials and methods. Using a single sample for thin-layer
cytology, HPV DNA-HR test and biomarkers, cytological diagnosis
has been made in a thin layer (ThinPrep) in a population
of women aged 25-64 aa HPV DNA-HR positive. In a second
step a survey for immunocytochemical study p16INK4a /ki67 has
been made. The simultaneous expression of two biomarkers in
the same cell of cervical epithelium is a morphology-independent
marker of deregulation of cell cycle. Using CINtec ® PLUS in pap
tests the positive staining for both proteins (p16 and Ki67) in the
same cell shows brown cytoplasm (over-expression of p16) and
red nucleus (Ki67 expression) (Fig. 1). The investigator with
CINtec ® PLUS (monoclonal mouse anti-Human p16INK4a antibody,
Clone E6H4TM , and monoclonal rabbit anti-Human Ki-67
antibody Clone 274-11 AC3) has been made on 951 cases. The
immunohystochemical analysis with primary monoclonal mouse
antibody clone E6H4 TM has been made on histological sections
CONGRESSO aNNualE di aNatOmia patOlOGiCa SiapEC – iap • fiRENzE, 25-27 OttOBRE 2012
Fig. 1
Results. Cytological correlation and investigation with CINtec ®
PLUS: co-expression of p16/Ki67 in individual cytological categories.
Among the negative cytological cases, 3.2% was positive,
while 96.8% negative. The positivity was confirmed after
review of the cases, performed by protocol. Among the cases
of ASC-US, 23% was positive at p16/Ki67 investigation. This
percentage may increase the VPP for CIN2+ in a diagnostic
category which does not seem easy to reproduce. Among
the LSIL cases, 27.2% was positive and therefore subject to
greater risk of progression to high grade lesions. The 72.8%
was found negative and therefore likely to get regression of
the cervical lesion. All the cytological HSIL cases and 76% of
ASC-H cases were positive in the survey p16/Ki67; all these
patients, after colposcopy and biopsy had high grade lesions.
197 cases with a histological follow-up (three months - six
months) and 84 cases with cytological follow-up have been
found. Histological diagnosis of high grade lesions were 51:
35 CIN2 (30 with cytology and P16/Ki67 positive and 5 with
cytology positive and P16/Ki67 negative) and 16 CIN3 (only
1 with cytology positive and P16/Ki67 negative); diagnosis of
low grade lesions were 101 (26 with cytology and P16/Ki67
positive and 75 with cytology positive and P16/Ki67 negative);
negative diagnosis were 45 (11 with cytology and P16/Ki67
positive and 34 with cytology positive and P16/Ki67 negative).
Conclusions. In cytological negative cases the investigation IIC
with CINtec ® PLUS can be a valuable support in the clinical
picture of atrophy / dystrophy (menopause) in which the morphology
of the “small cells” can give false negatives. Increased
sensitivity of the cytological test. In ASC-US and LSIL it is essential
to distinguish lesions with significant risk of progression
to CIN2 / 3, which will require a shorter- term follow up. The
same diagnostic categories which are negative at biomarkers regress
spontaneously and / or rarely progress. For this reason it is
possible to reduce the risk of over-treatment and to plan a longterm
follow-up. In cases of ASC-H and HSIL the investigation
IIC with CINtec ® PLUS confirms the presence of high-grade
and high risk of progression lesions. However in a low percentage
it is essential a further study of biomarkers.
Fig. 2